Anesth Analg 2001;93:1132-1134
© 2001 International Anesthesia Research Society
CARDIOVASCULAR ANESTHESIA
Left-Sided Cardiac Gas Embolism Produced by Hydrogen Peroxide: Intraoperative Diagnosis Using Transesophageal Echocardiography
José A. Sastre, MBBS,
María A. Prieto, MBBS,
José C. Garzón, MBBS, and
Clemente Muriel, MD
Anesthesiology Service, University Hospital of Salamanca, Salamanca, Spain
Address correspondence and reprint requests to José Alfonso Sastre Rincón, MBBS, Servicio de Anestesiología, Hospital Universitario de Salamanca, Paseo de San Vicente, 58-182, 37007, Salamanca, Spain. Address e-mail to med026221{at}nacom.es
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Abstract
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IMPLICATIONS: We present a case of an adult who suffered a left-sided gas embolism after surgical lavage of the thoracic cavity with hydrogen peroxide. An intraoperative diagnosis was made using transesophageal echocardiography.
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Introduction
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The use of transesophageal echocardiography (TEE) in cardiac surgery permits the evaluation of cardiac anatomy and function and can also be used to diagnose intracardiac shunts, disturbances in valvular function, gas embolism, aortic dissection, and myocardial ischemia (1). TEE can also be a useful technique for detecting problems that occur during the anesthetic or surgical actions.
Hydrogen peroxide (H2O2) is an oxidizing agent commonly used in wound cleansing because of its germicidal action and, in addition, for its action in bubbling out foreign materials and debris (2). However, its administration has been associated with gas embolism in a variety of procedures (3–10).
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Case Report
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A 78-yr-old, 52-kg woman with mitral and aortic valvular disease and chronic atrial fibrillation was scheduled for replacement of both valves with biological Carpentier protheses. After a normal postoperative course, the patient returned to the intensive care unit a week later because of severe anemia and respiratory insufficiency caused by a massive right hemothorax. Thoracic drainage and blood transfusion were performed, followed by an exploratory sternotomy. Anesthesia was induced with IV fentanyl 0.15 mg, etomidate 12 mg, and rocuronium bromide 30 mg. Maintenance included fentanyl infusion 4 µg · kg-1 · h-1, propofol 4 mg · kg-1 · h-1, rocuronium bromide 0.5 mg · kg-1 · h-1, and O2/N2O. Intraoperative monitors included electrocardiogram (ECG) leads II and V5 with ST segment analysis, invasive blood pressure, central venous pressure, pulse oximetry, urine output, muscle relaxation, capnography (PETCO2), and TEE by an omniplanar probe (HP Omniplana II 21369Aand Hewlett-Packard Image Point HX; Hewlett-Packard, Andover, MA). After sternal incision, blood and clots were found in the right pleural cavity without an active source of hemorrhage. Examination of the surgical wound disclosed a small tear on the anterior surface of the middle lobe. Before chest closure, the surgeon irrigated the surgical field with 300 mL 1% H2O2 solution. Immediately, a ST segment increase of 3.2 mm was observed in ECG leads II, III and aVF. Coronary vasospasm was suspected. Nitroglycerin 50 µg IV was administered, followed by an infusion at a rate of 20 µg · kg-1 · min-1. Two minutes later the patient suffered a severe decrease in blood pressure, bradycardia of 30 bpm, a decrease in pulse oximetry value from 95% to 89%, and a decrease in PETCO2 from 34 mm Hg to 30 mm Hg. Atropine 1 mg and ephedrine 10 mg IV were given. Air bubbles were detected by TEE in left-side structures (Fig. 1, 2). The diagnosis of gas embolism was strongly suspected. One-hundred percent oxygen was administrated and the surgical field was flooded with saline solution. The patient was placed in the Trendelenburg position to aid in removing gas from the left ventricle by placement of a needle into the apex. Just before insertion of the needle, sudden asystole occurred. Internal cardiac massage was initiated and epinephrine 1 mg IV was given. Within seconds, the patient’s ventricular rate increased to 50 bpm and a small amount of air bubbles exited the left ventricle through the needle. Epicardial electrodes were connected to a pacemaker to increase the heart rate to 80 bpm. In a few minutes ECG abnormalities disappeared and the patient recovered hemodynamic stability. After chest closure, the patient was transferred to the intensive care unit and was tracheally extubated 1 h later. Follow-up evaluation showed no evidence of neurologic deficit and no increase of serum cardiac markers. The subsequent clinical course was favorable and the patient was discharged from the hospital 15 days later.
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Figure 1. 1, Left atria; 2, left pulmonary vein; 3, air bubbles in left atria; 4, left ventricle with air bubbles; 5, Carpentier bioprosthesis; 6, right atria without air bubbles.
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Figure 2. 1, left atria; 2, air bubbles in left atria; 3, Carpentier bioprosthesis; 4, left ventricle with air bubbles; 5, right atria without air bubbles.
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Discussion
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Gas embolism produced by hydrogen peroxide is an uncommon surgical complication that can be explained by a chemical reaction in which hydrogen peroxide decomposes rapidly as a result of the action of catalases in blood and tissues, releasing molecular oxygen and H2O:
It has been calculated that 1 mL of H2O2 3% produces 10 mL of oxygen in the tissues (3).
Air embolism produced by H2O2 has been typically associated with injection under pressure into closed and semiclosed body cavities (7–9). However, life-threatening complications have been reported using H2O2 for surgical lavage of open wounds (4,5,10), as well as after accidental acute oral poisoning in children (11). Nascent oxygen molecules released lead to absorption into venous plexus and cause right ventricle collapse and decreased cardiac output. Some of these air bubbles may reach the lungs and, even, produce paradoxic embolism through an interatrial or ventricular shunt (12). The classic signs are hypotension, bradycardia, cardiac arrest, a precordial "mill-wheel" murmur, and a sharp decrease in PETCO2 and oxygen saturation. As diagnostic methods we can use precordial auscultation for "mill-wheel" murmur, TEE (13), precordial Doppler, and measurement of pulmonary artery pressure and right ventricle output. Treatment of an air embolism should include the following: a) rinsing the surgical field or the point of gas entry with saline solution; b) placing the patient in the Trendelenburg and left lateral position to trap gas in the apex of the ventricle where it can be evacuated through a venous catheter (right-sided embolism) or by placement of a needle into the apex (left-sided embolism); c) administration of 100% oxygen; d) administration of inotropic drugs and other life-support measures to maintain hemodynamic stability; e) use of hyperbaric therapy or nitric oxide (14).
In our case, the diagnosis was suggested by a sudden alteration in hemodynamic variables and the evidence of air in the left heart structures. Bedell et al. (15) demonstrated the evidence of transpulmonary air passage using TEE in a patient who underwent intracranial vascular surgery and postulated that significant increase of pulmonary artery pressure during venous embolism could open intrapulmonary shunts that normally remain closed. The existence of transpulmonary air passage seems to be determined by the volume of gas, as demonstrated by Butler and Hills (16) in a canine model. Some situations, such as lung disease and positive-pressure ventilation, might increase the risk of paradoxical embolism in the absence of a demonstrable right-to-left intracardiac shunt (4). In our patient we did not notice air bubbles in the right heart cavities, so we suspected that the pulmonary vasculature was the source of the left-sided air. In preoperative studies including right and left cardiac catheterization and TEE, there was no evidence of intracardiac shunting. At the end of the surgery we tried unsuccessfully to find an atrial septal defect by a Valsalva maneuver with 20 cm H2O positive end-expiratory pressure and injection of agitated saline, an effective test to exclude an interatrial defect (17). Although we cannot absolutely exclude a paradoxic embolism, we think that this case most likely was a direct left-sided air embolism. We believe that hydrogen peroxide entered the pulmonary venous circulation through the tear in the lobe and then flowed into the left atrium. The ST segment increase in ECG leads II, III, and aVF could be explained by passage of air bubbles into the right coronary artery, which is situated superiorly when the patient is placed in the supine position (18).
In our patient, the use of TEE permitted rapid diagnosis of an intraoperative complication. Although the patient had an uneventful recovery, it is important to remember that the intraoperative use of H2O2 has been associated with near-fatal catastrophes and perhaps should be avoided as a surgical lavage solution.
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References
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Accepted for publication June 13, 2001.
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Abstract
Introduction
